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Published on: September 9, 2020
Pinocembrin prevents glutamate-induced apoptosis in SH-SY5Y neuronal cells via decrease of bax/bcl-2 ratio
Mei Gao1, Wen-Cui Zhang, Qing-Shan Liu
1Institute of Materia Medica, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100050, China.
European Journal of Pharmacology
|July 16, 2008
Summary
Pinocembrin, a propolis flavonoid, protects neurons from glutamate injury by reducing apoptosis and calcium influx. It achieves this by inhibiting p53 expression and cytochrome c release, offering potential neuroprotection.
Area of Science:
- Neuroscience
- Pharmacology
- Biochemistry
Background:
- Pinocembrin, a major propolis flavonoid, exhibits antioxidant, antibacterial, and anti-inflammatory properties.
- Glutamate excitotoxicity is a significant factor in neuronal damage and neurodegenerative diseases.
- Understanding the neuroprotective mechanisms of natural compounds like pinocembrin is crucial for therapeutic development.
Purpose of the Study:
- To investigate the neuroprotective effects of pinocembrin against glutamate-induced neuronal injury.
- To elucidate the molecular mechanisms underlying pinocembrin's protective actions in a neuronal cell model.
Main Methods:
- SH-SY5Y neuronal cells were pretreated with pinocembrin and subsequently exposed to glutamate.
- Cell viability was assessed using MTT assay; apoptosis was evaluated via cell morphology, capillary zone electrophoresis, and flow cytometry.
- Intracellular calcium levels, LDH release, and the expression of key apoptosis-related genes (Bax, Bcl-2) and proteins (p53, Bax, Bcl-2, cytochrome c) were analyzed.
Main Results:
- Pinocembrin dose-dependently increased cell viability, inhibited lactate dehydrogenase (LDH) release, and attenuated apoptosis in glutamate-treated cells.
- Pinocembrin reduced glutamate-induced intracellular calcium ([Ca2+]) increase and decreased the expression of Bax mRNA and protein, lowering the Bax-Bcl-2 ratio.
- Pinocembrin treatment down-regulated p53 protein expression and inhibited the release of cytochrome c from mitochondria to the cytosol.
Conclusions:
- Pinocembrin demonstrates significant neuroprotective effects against glutamate-induced neuronal injury in vitro.
- The neuroprotection is mediated partly through the inhibition of p53 expression, modulation of the Bax-Bcl-2 ratio, and prevention of cytochrome c release.
- These findings highlight pinocembrin as a potential therapeutic agent for conditions involving excitotoxic neuronal damage.
